Frontiers in Molecular Biosciences (Oct 2022)

Involvement of shedding induced by ADAM17 on the nitric oxide pathway in hypertension

  • Mirelly Cunha da Silva,
  • Vanessa Maria dos Santos,
  • Matheus Vinícius B. da Silva,
  • Tereza Cristina M. M. Prazeres,
  • Maria do Socorro S. Cartágenes,
  • Natália Tabosa M. Calzerra,
  • Thyago Moreira de Queiroz

DOI
https://doi.org/10.3389/fmolb.2022.1032177
Journal volume & issue
Vol. 9

Abstract

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A Disintegrin and Metalloprotease 17 (ADAM17), also called tumor necrosis factor-ɑ (TNF-ɑ) convertase (TACE), is a well-known protease involved in the sheddase of growth factors, chemokines and cytokines. ADAM17 is also enrolled in hypertension, especially by shedding of angiotensin converting enzyme type 2 (ACE2) leading to impairment of angiotensin 1–7 [Ang-(1–7)] production and injury in vasodilation, induction of renal damage and cardiac hypertrophy. Activation of Mas receptor (MasR) by binding of Ang-(1–7) induces an increase in the nitric oxide (NO) gaseous molecule, which is an essential factor of vascular homeostasis and blood pressure control. On the other hand, TNF-ɑ has demonstrated to stimulate a decrease in nitric oxide bioavailability, triggering a disrupt in endothelium-dependent vasorelaxation. In spite of the previous studies, little knowledge is available about the involvement of the metalloprotease 17 and the NO pathways. Here we will provide an overview of the role of ADAM17 and Its mechanisms implicated with the NO formation.

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